Cerebral palsy.

The clinical pattern and etiology of 544 cases of cerebral palsy were studied retrospectively. Of these cases, 354 (65.1%) were males. Four hundred and ninety seven (91.4%) cases were of spastic type. Hypotonic, ataxic and athetoid cerebral palsy were observed in 5.5, 1.5 and 1.3% cases, respectively. There was one case each of tremor and mixed type. In the spastic group, quadriplegia comprised the maximum number of cases (34.9%). Hemiplegia (28.7%) and diplegia (21.9) were also common. Mental retardation was found in 47.2%, while speech impairment was observed in 37% cases. Other handicaps included visual (9%), seizures (8.8%), and auditory handicap (2.9%). The etiological factors were prenatal in 7.7% cases, natal in 43.8% cases and postnatal in 26.1% cases. More than one etiological factor was observed in 14.5% cases, while in 7.9% cases, no apparent cause could be found.     

Cerebral oxygenation during subclinical seizures in neonatal hypoxic-ischaemic encephalopathy

Treatment of subclinical seizures in newborn HIE remains a contentious issue, especially in light of potential adverse effects of aggressive use of anticonvulsants. We report on the association of subclinical seizures with changes in cerebral oxygenation in an infant with HIE. Our results show that subclinical seizures of longer durations and with associated autonomic disturbance (increased blood pressure) are more likely to be associated with fluctuation in cerebral oxygenation, with some seizures resulting in cerebral hypoxia. Future studies should aim to delineate the effects of subclinical seizure and anticonvulsant treatment on cerebral oxygenation, and their relationships to developmental outcome. Level of cerebral oxygenation may play a role in refining anti-convulsant treatment and management of subclinical seizures in newborns.     

Cerebral palsy and congenital malformations.

AIM: To determine the proportion of children with cerebral palsy (CP) who have cerebral and non-cerebral congenital malformations. METHODS: Data from 11 CP registries contributing to the European Cerebral Palsy Database (SCPE), for children born in the period 1976-1996. The malformations were classified as recognized syndromes, chromosomal anomalies, cerebral malformations or non-cerebral malformations. Prevalence of malformations was compared to published data on livebirths from a European database of congenital malformations (EUROCAT). RESULTS: Overall 547 out of 4584 children (11.9%) with CP were reported to have a congenital malformation. The majority (8.6% of all children) were diagnosed with a cerebral malformation. The most frequent types of cerebral malformations were microcephaly and hydrocephaly. Non-cerebral malformations were present in 97 CP children and in further 14 CP children with cerebral malformations. The most frequent groups of non-cerebral malformations were cardiac, facial clefts and limb and skeleton malformations. Children born at term had a significantly higher prevalence of cerebral malformations compared to children born before 32 weeks (12.1% versus 2.1%, p<0.001). CONCLUSION: Cerebral malformations were much more frequent among children with CP than among all livebirths in the population. Malformations in organ systems close to the brain (eye, facial clefts) were more frequent in the CP population while malformations in organ systems further from the brain (renal, genital) were more frequent in the general population.     

Cerebral palsy and multiple births.

AIM: To compare the birthweight specific prevalence of cerebral palsy in singleton and multiple births. METHODS: Registered births of babies with cerebral palsy born to mothers resident in the counties of Merseyside and Cheshire during the period 1982 to 1989 were ascertained. RESULTS: The crude prevalence of cerebral palsy was 2.3 per 1000 infant survivors in singletons, 12.6 in twins, and 44.8 in triplets. The prevalence of cerebral palsy rose with decreasing birthweight. The birthweight specific prevalence among those of low birthweight < 2500 g was not significantly different in singleton than in multiple births. Among infants weighing > or = 2500 g, there was a significantly higher risk in multiple than in singleton births. The higher crude cerebral palsy prevalence in multiple births is partly due to the lower birthweight distribution and partly due to the higher risk among normal birthweight infants. CONCLUSIONS: Multiple birth babies are at increased risk of cerebral palsy. There is also an increased risk of cerebral palsy within a twin pregnancy if the co-twin has died in utero.     

Term neonatal encephalopathy antecedent cerebral palsy: A retrospective population-based study

ObjectiveTo compare the clinical profile of term-born cerebral palsy children with or without antecedent moderate to severe neonatal encephalopathy. We hypothesized that antecedent neonatal encephalopathy is associated with a spastic quadriparesis cerebral palsy clinical profile, a higher severity of functional motor impairment, and a greater number of associated comorbidities.MethodsUsing the Quebec Cerebral Palsy Registry, neurologic subtype, Gross Motor Function Classification System stratification, and comorbidities were compared in children with cerebral palsy with and without antecedent neonatal encephalopathy. Differences between groups were evaluated using chi square analysis for categorical variables and student t test for continuous variables.ResultsWe identified 132 children with cerebral palsy born full term over a 4 year-interval (1999–2002 inclusive) within the Quebec Cerebral Palsy Registry, of which 44 (33%) had an antecedent neonatal encephalopathy. Spastic quadriplegia subtype of cerebral palsy and Gross Motor Function Classification System Level III–V (non-independent ambulation) were significantly associated with antecedent neonatal encephalopathy. The mean number of comorbidities experienced was not different in the two groups. Of five documented comorbidities, only severe communication difficulties were found to be associated (p < 0.05) with antecedent neonatal encephalopathy.ConclusionA pattern of increased neuromotor impairment, functional gross motor severity and possible communication difficulties was found in the 33% of children with cerebral palsy born at term and with a history of neonatal encephalopathy.     

Cerebral palsy

Epidemiology of cerebral palsy is complex, being influenced by various factors, some of which are unknown and it is commonly accompanied by other abnormalities, thus involving a variety of specialization in their treatment. In a period of 1978-1985, a retrospective study of cerebral palsy cases was performed at the Child Neurology Subdivision Department of Child Health School of Medicine, University of Sumatera/Dr. Pirngadi Hospital, Medan. There were 40 cases (1.59%) out of 2,505 new child neurological cases, consisting of 20 males (50%) and 20 females (50%). The youngest was 4 months and the oldest was 7 years and 5 months of age. Thirty two cases (80%) appeared predominantly with the age less than 3 years. The predominant cause was neonatal asphyxia in 11 cases (27.5%), the uncertain causes were found 8 cases (20%). Spastic cerebral palsy was found in 28 cases (70%) and there were 13 cases (32.5%) accompanied by microcephaly.     

Cerebral intracellular lactic alkalosis persisting months after neonatal encephalopathy measured by magnetic resonance spectroscopy.

We have found that cerebral lactate can be detected later than 1 month of age after neonatal encephalopathy (NE) in infants with severe neurodevelopmental impairment at 1 y. Our hypothesis was that persisting lactate after NE is associated with alkalosis and a decreased cell phosphorylation potential. Forty-three infants with NE underwent proton and phosphorus-31 magnetic resonance spectroscopy at 0.2-56 wk postnatal age. Seventy-seven examinations were obtained: 25 aged <2 wk, 16 aged > or = 2 to < or = 4 wk, 25 aged > 4 to < or = 30 wk, and 11 aged > 30 wk. Neurodevelopmental outcome was assessed at 1 y of age: 17 infants had a normal outcome and 26 infants had an abnormal outcome. Using univariate linear regression, we determined that increased lactate/creatine plus phosphocreatine (Cr) was associated with an alkaline intracellular pH (pHi) (p < 0.001) and increased inorganic phosphate/phosphocreatine (Pi/PCr) (p < 0.001). This relationship was significant, irrespective of outcome group or age at time of study. Between outcome groups, there were significant differences for lactate/Cr measured at < 2 wk (p = 0.005) and > 4 to < or = 30 wk (p = 0.01); Pi/PCr measured at < 2 wk (p < 0.001); pHi measured at < 2 wk (p < 0.001), > or = 2 to < or = 4 wk (p = 0.02) and > 4 to < or = 30 wk (p = 0.03); and for N-acetylaspartate/Cr measured at > or = 2 to < or = 4 wk (p = 0.03) and > 4 to < or = 30 wk (p = 0.01). Possible mechanisms leading to this persisting cerebral lactic alkalosis are a prolonged change in redox state within neuronal cells, the presence of phagocytic cells, the proliferation of glial cells, or altered buffering mechanisms. These findings may have implications for therapeutic intervention.     

Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy

Neonatal encephalopathy (NE) is the clinical manifestation of disordered neonatal brain function. Lack of universal agreed definitions of NE and the sub-group with hypoxic-ischaemia (HIE) makes the estimation of incidence and the identification of risk factors problematic. NE incidence is estimated as 3.0 per 1000 live births (95%CI 2.7 to 3.3) and for HIE is 1.5 (95%CI 1.3 to 1.7). The risk factors for NE vary between developed and developing countries with growth restriction the strongest in the former and twin pregnancy in the latter. Potentially modifiable risk factors include maternal thyroid disease, receipt of antenatal care, infection and aspects of the management of labour and delivery, although indications for some interventions were not reported and may represent a response to fetal compromise rather than the cause. It is estimated that 30% of cases of NE in developed populations and 60% in developing populations have some evidence of intrapartum hypoxic-ischaemia.     

Cerebral palsy and communication

Cerebral palsy (CP) can cause disturbances in sensory and cognitive development as well as motor disorders. Problems in these areas of functioning can affect children’s speech, language and communication development. The intelligibility of children’s speech, gesture and the communication signals expressed by body movement may be reduced, and children’s expression and understanding of language can be delayed. This review describes the communication difficulties commonly associated with CP, their assessment by speech and language therapists, and the interventions that may be employed to reduce their impact on children’s activity and participation.     

Cerebral palsy and neurodegenerative disease

Cerebral palsy refers to a neurologic disorder of motor skills that is static in nature and is the result of injury to the brain before its development is complete. Many neurodegenerative or metabolic disorders have a slow rate of progression and can be misdiagnosed as cerebral palsy. Diseases that have been misdiagnosed as cerebral palsy are presented here to provide the clinician with framework for the complex evaluation of these patients.     

Cerebral palsy in children

Summary The present study includes 50 cases of cerebral palsy. The possible etiological factors were forceps application or caeserean section in 7 cases, neonatal jaundice in 2 cases, neonatal hypoxia in 3 cases, breech delivery in 2 cases, history of high fever and convulsions in 2 cases, head injury in 4 cases, premature and post mature delivery in 4 cases and in one case the child did not cry for 2 days. Of the neurological types there were 32 cases of spasticity, 5 cases of athetosis, 6 cases of ataxia, 6 cases of hypotonia and one was of the mixed type. The literature is briefly reviewed. From the Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, New Delhi-16.     

Cerebral palsy in very low birthweight infants.

Eighty one very low birthweight survivors with cerebral palsy were matched with controls by sex, gestational age, and place of birth. Using discriminant analysis, the perinatal profiles for infants with cerebral palsy and their controls were shown to differ significantly. When infants with various types of cerebral palsy were analysed with their controls the discriminating variables differed. Diplegic infants could be differentiated from controls on antenatal variables alone, but significant discrimination of hemiplegic and quadriplegic infants required the addition of postnatal variables. Cranial ultrasound appearances differed appreciably between types of cerebral palsy. Future studies should differentiate between types of cerebral palsy and include ultrasound data. Cerebral palsy in very low birthweight infants is unlikely to prove a useful outcome indicator for neonatal intensive care.